Serotonin is a neurotransmitter largely responsible for emotional response and believed, by the inventors, to play a key role in the transmission of pain impulses from the source of the pain to the brain. As such, conditions such as PMS, perimenopause, menopause/post-menopause, seasonal affective disorder, stress, and depression may be aggravated when the brain experiences a serotonin deficiency. Tryptophan is a precursor to serotonin and it competes with other large neutral amino acids (LNAA) for transport into the brain. Thus, others have attempted to increase brain serotonin by raising the ratio of tryptophan to LNAA in the blood through various mechanisms.
One mechanism taught in the prior art uses an insulin response, such as is triggered by the consumption of carbohydrates. Literature suggests that this mechanism works best when protein is absent and/or at low levels. For example, one published study states “As little as 2–4% of the calories of a meal as protein will prevent an increased availability of tryptophan”, Benton, D. & Donohoe, R. T, “The Effects of Nutrients on Mood”, Public Health Nutrition, Vol. 2(3a), pp. 403–409 (1999). The insulin response encourages some portion of LNAA to leave the blood stream and enter skeletal muscle. Tryptophan is more resistant than the other LNAA to entering skeletal muscle, with proportionally more staying in the blood. The result is a relatively higher ratio of tryptophan:LNAA in the blood.
The second mechanism for increasing the tryptophan:LNAA ratio is to tailor diets to comprise proteins that are rich in tryptophan relative to other LNAA, with the idea that as the relative amount of tryptophan available in the protein goes up, the tryptophan:LNAA ratio in the blood will also go up. One study dosed a high tryptophan containing whey protein with carbohydrate (orange juice) and either 25 or 50 g of glucose, Markus, C. R. et al., “Dose-Dependent Effect of α-Lactalbumin in Combination with Two Different Doses of Glucose on the Plasma Trp/LNAA Ratio”, Nutritional Neuroscience, Vol. 3, pp. 345–355 (2000). The study concluded that the different glucose doses did not influence the tryptophan:LNAA ratio. The study also concluded that “since insulin responses across time did not significantly differ between the different α-lactalbumin conditions differences in the time dependent effects between these α-lactalbumin conditions on plasma Trp/LNAA do not seem to depend on insulin alterations” (page 353).
Notwithstanding these teachings, it has been surprisingly found that the use of both mechanisms together actually enhances the effectiveness in raising the tryptophan:LNAA ratio in blood. The inventors of the current invention have discovered a dosage regimen that provides a tryptophan:LNAA ratio boost when relatively low levels of carbohydrates and a high tryptophan containing protein are administered.